Cancer Res.：吸烟损害精子质量
生物谷报道：据新一期美国《癌症研究》月刊报道，“健康加拿大”组织和加拿大麦克马斯特大学科研人员以实验鼠为研究对象，让它们暴露于烟雾环境中。如果按烟雾在血液中的含量计算，实验鼠吸入的烟雾量相当于普通吸烟者的水平。
研究发现，“吸烟”可导致实验鼠的精原干细胞发生变化，其精液基因序列中的基因Ｍｓ６－ｈｍ因“吸烟”而遭到了破坏。对于“吸烟”６周的实验鼠来说，精液中Ｍｓ６－ｈｍ基因发生变异的几率比未“吸烟”实验鼠高１．４倍；而“吸烟”１２周的实验鼠，这一数字为１．７倍。这些实验鼠生育的后代精原干细胞也出现了基因变异现象。
科研人员指出，实验证明，“吸烟”时间越长，实验鼠的精原干细胞受破坏的程度越高，同时就越有可能将受破坏的基因遗传给后代。
负责这项研究的科学家卡萝尔·尤克表示，“众所周知，母亲吸烟会影响胎儿，现在我们有证据表明，父亲吸烟也会危害后代”。尤克指出，雄性动物，不管是人还是老鼠，都要靠精原干细胞源源不断地生产新精子，如果精原干细胞受到破坏，精子的数量和质量就要受到影响。
过去的研究曾发现，辐射、工业污染和一些化学物质可导致男性精原干细胞中的Ｍｓ６－ｈｍ基因发生变异。
原始出处:
Cancer Research 67, 5103-5106, June 1, 2007. doi: 10.1158/0008-5472.CAN-07-0279
Priority Reports
Mainstream Tobacco Smoke Causes Paternal Germ-Line DNA Mutation
Carole L. Yauk1, M. Lynn Berndt1, Andrew Williams2, Andrea Rowan-Carroll1, George R. Douglas1 and Martin R. Stämpfli3
1 Mutagenesis Section, Environmental and Occupational Toxicology Division; 2 Biostatistics and Epidemiology Division, Health Canada, Ottawa, Ontario, Canada; and 3 Department of Pathology and Molecular Medicine, Centre for Gene Therapeutics and Department of Medicine, McMaster University, Hamilton, Ontario, Canada
Requests for reprints: Carole L. Yauk, Environmental Health Centre, Tunney's Pasture, Postal locator 0803A, Ottawa, Ontario, Canada. Phone: 613-941-7376; Fax: 613-941-8530; E-mail: carole_yauk@hc-sc.gc.ca .
Despite the presence of known mutagens and carcinogens in cigarette smoke, there is currently no evidence to show that smoking, or exposure to cigarette smoke, can result in heritable genetic mutation. We show that male mice exposed to mainstream tobacco smoke (MTS) exhibit a significant increase in germ-line mutation frequency in spermatogonial stem cells. We exposed mature male mice to MTS for 6 or 12 weeks and investigated mutations arising in exposed spermatogonial stem cells at the expanded simple tandem repeat locus Ms6-hm. A generalized score test showed a significant treatment effect (P = 0.0214). Ms6-hm mutation frequency was 1.4 and 1.7 times higher in mice exposed to MTS for 6 and 12 weeks, respectively, compared with sham controls. The data suggest that mutations accumulate in the spermatogonial stem cells with extended exposures. Mutation spectra were identical between exposed and sham individuals, supporting the hypothesis that tandem repeat mutations arise through indirect mechanisms of mutation. Mutations in sperm that are passed on to offspring cause permanent, irreversible changes in genetic composition and can persist in future generations. Our research suggests that the consequences of smoking extend beyond the smoker to their nonsmoking descendents. [Cancer Res 2007;67(11):5103–4]
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